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KMID : 1140120070120040256
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Cancer Prevention Research
2007 Volume.12 No. 4 p.256 ~ p.260
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Study on the Chemopreventive Mechanism of Selenium in Terms of the Activation of p53 Tumor Suppressor and PTEN
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Jung Hwa-Jin
Seo Young-Rok
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Abstract
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Selenomethionine (SeMet) has been identified as one of the organic selenium compounds although the mechanism of chemopreventive action of SeMet was not clear yet. In our previous study, we suggested that p53 might be involved in chmopreventive effect of SeMet. Here, we investigated the implication of the p53 modulated by redox signal in response to SeMet in cancer prevention. We confirmed that the p53 accumulation was significantly increased in response to SeMet as dose-dependent manner. In addition, the differential localization of p53 protein was observed in nucleolus contrast with in redox factor 1 (Ref-1)-dominant negative cells indicating that p53 function for genomic stability might be modulated by redox signaling. On the other hand, PTEN known as a tumor suppressor with the inhibition of PI3K/Akt signaling pathway has no significant differences in the presence with SeMet suggesting that the chemopreventive mechanism of SeMet might be on PTEN-independent pathway. In our study, we suggested that p53 activation and localization in nucleolus might be a distinct cellular pathway of SeMet as one of the chemopreventive compounds. (Cancer Prev Res 12, 256-260, 2007)
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KEYWORD
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p53, PTEN, Selenomethionine
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